title: Increased activity of group II phospholipase A2 in plasma in rat sodium deoxycholate induced acute pancreatitis.
abstract: BACKGROUND
  Two different types of secretory phospholipase A2 (PLA2), pancreatic group I (PLA2-I) and non-pancreatic group II (PLA2-II), have been identified and postulated to be associated with the pathogenesis of various diseases, such as acute pancreatitis, septic shock, and multiple organ failure.
  
  
  OBJECTIVE
  To investigate the type of secretory PLA2 responsible for its catalytic activity found in plasma and ascites of experimental acute pancreatitis.
  
  
  METHODS
  Acute pancreatitis of differing severity was induced by the injection of different concentrations (1% or 10%) of sodium deoxycholate (DCA) into the common biliopancreatic duct in rats, and catalytic PLA2 activity in plasma and ascites were differentiated by anti-PLA2-I antibody and specific inhibitor of PLA2-II. Survival rate and plasma amylase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were also measured.
  
  
  RESULTS
  In 1% and 10% DCA induced acute pancreatitis, plasma amylase values as well as PLA2 activity in ascites were greatly increased. PLA2 activity in plasma was also notably increased in 10% DCA induced acute pancreatitis, but not in 1% DCA induced acute pancreatitis. PLA2-I specific polyclonal antibody significantly inhibited PLA2 activity in ascites but not that in plasma. In contrast, plasma PLA2 activity was completely suppressed by PLA2-II specific inhibitor. In addition, a high mortality (93% at five hours) and a significant increase in plasma AST and ALT were noted in 10% DCA induced pancreatitis.
  
  
  CONCLUSIONS
  Ascites PLA2 activity is mainly derived from PLA2-I, whereas plasma PLA2 activity is mostly derived from PLA2-II in severe acute pancreatitis, suggesting that increased plasma PLA2-II activity might be implicated in hepatic failure arising after severe acute pancreatitis.
authors.affiliation: Discovery Research Laboratories II, Shionogi & Co. Ltd, Osaka, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Furue
authors.forename: Y
authors.initials: Y
authors.lastname: Hori
authors.forename: K
authors.initials: K
authors.lastname: Kuwabara
authors.forename: J
authors.initials: J
authors.lastname: Ikeuchi
authors.forename: H
authors.initials: H
authors.lastname: Onoyama
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
mesh_terms: D000208:Acute Disease; D000410:Alanine Transaminase / Q000097:blood; D000681:Amylases / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001681:Biological Assay; D002756:Cholagogues and Choleretics; D003840:Deoxycholic Acid; D054501:Group II Phospholipases A2; D017093:Liver Failure / Q000201:enzymology*; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000201:enzymology* / Q000401:mortality; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D051381:Rats; D017208:Rats, Wistar; D015996:Survival Rate
chemical_list: D002756:Cholagogues and Choleretics; D003840:Deoxycholic Acid; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D010741:Phospholipases A; D054501:Group II Phospholipases A2; D054467:Phospholipases A2; D000681:Amylases